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How The Thyroid System Works
REFERENCE: Wikipedia - Thyroid
The thyroid is one of the larger endocrine glands in the body. It is located in the neck and produces hormones, principally thyroxine (T4) and triiodothyronine (T3), that regulate the rate of metabolism and affect the growth and rate of function of many other systems in the body.
The thyroid is composed of spherical follicles that selectively absorb iodine (as iodide ions, I-) from the blood and for production of thyroid hormones. Twenty-five percent of all the body I- is in the thyroid gland. The follicles are made of a single layer of thyroid epithelial cells, which secrete T3 and T4. Inside the follicles is a colloid which is rich in a protein called thyroglobulin. The colloidal material serves as a reservoir of materials for thyroid hormone production and, to a lesser extent, a reservoir of the hormones themselves.
he primary function of the thyroid is production of the hormones thyroxine (T4), triiodothyronine (T3), and calcitonin. Up to 40% of the T4 is converted to T3 by peripheral organs such as the liver, kidney and spleen. T3 is about ten times more active than T4.
T3 and T4 Production and Action
Thyroxine is synthesised by the follicular cells from the tyrosine residues of the protein called thyroglobulin (TG). Iodine, captured with the "iodine trap" is activated by the enzyme thyroid peroxidase (TPO) and linked to the 3' and 5' sites of the benzene ring of the tyrosine residues on TG. Upon stimulation by TSH (see below), the follicular cells reabsorb TG and proteolytically cleave the iodinated tyrosines from TG, forming T4 and T3 (in T3, one iodine is absent compared to T4), and releasing them into the blood. Thyroid hormone that is secreted from the gland is about 90% T4 and about 10% T3.
Cells of the brain are a major target for thyroid hormone. A transport protein (OATP1C1) has been identified that seems to be important for T4 transport across the blood brain barrier. A second transport protein (MCT8) is important for T3 transport across brain cell membranes.
In the blood, T4 and T3 are partially bound to thyroxine-binding globulin, transthyretin and albumin. Only a very small fraction of the circulating hormone is free (unbound) - T4 0.03% and T3 0.3%. Only the free fraction has hormonal activity. As with the steroid hormones and retinoic acid, thyroid hormones cross the cell membrane and bind to intracellular receptors (α1, α2, β1 and β2), which act alone, in pairs or together with the retinoid X-receptor as transcription factors to modulate DNA transcription.
T3 and T4 Regulation
The production of thyroxine is regulated by thyroid-stimulating hormone (TSH), released by the pituitary. The thyroid and thyrotropes form a negative feedback loop: TSH production is suppressed when the T4 levels are high, and vice versa. The TSH production itself is modulated by thyrotropin-releasing hormone, which is produced by the hypothalamus and secreted at an increased rate in situations such as cold (in which an accelerated metabolism would generate more heat). TSH production is blunted by somatostatin (SRIH).
Scientists now consider thyroid hormone one of the major “players” in brain chemistry disorders. And as with any brain chemical disorder, until treated correctly, thyroid hormone imbalance has serious effects on the patient’s emotions and behavior.
Once the important thyroid hormones, T3 and T4, are released into your bloodstream, they enter cells of organs and play an important role in regulating major functions in the body. Adequate amounts of thyroid hormone are also required throughout your life if your brain is to function normally. Most of your cognitive abilities — such as concentration, memory, and attention span — as well as mood and emotions depend on normal thyroid hormone levels. Mounting evidence suggest that T3, the most potent form of thyroid hormone, is a bona fide brain chemical. It is found in the junction of nerve (synapse) cells that allow these cells to communicate with one another. This thyroid hormone also regulates the levels and actions of serotonin, noradrenaline, and GABA (gamma-aminobutyric acid), now accepted as the main chemical transmitters implicated in both depression and some anxiety disorders. Maintaining normal serotonin and noradrenaline levels in the brain depends to a great extent on whether the correct amount of T3 is available. Extensive animal and human research has led scientists to conclude that serotonin levels in the brain decrease if T3 is not delivered in the right amount. Also, a deficit of T3 in the brain is likely to result in noradrenaline’s working inefficiently as a chemical transmitter, and noradrenaline deficiency or inefficiency is, in some people, the chemical reason for depression.
“…Thyroid patients, particularly those with hypothyroidism, want peace and quiet. They feel the need to withdraw from activity and noise. They have a low tolerance for sound. In essence, they wish to insulate themselves in a surrealistic world of tranquility.”
”Patients may become withdrawn from friends, and they do not want to talk or go out with people. They may lose all interest in doing things with their partners… Hypothyroid patients want to be left alone. They just want to sleep and withdraw from those around them. In some cases, they realize the people around them are doing the best they can, but they still want to maintain their isolation.”
What are some of the behavioral and psychiatric symptoms of a low thyroid condition in the brain?
Depression, anxiety, panic attacks, agoraphobia, obsessive compulsive tendencies, ultra-sensitive to the comments of others, social phobia, self-image concerns, unable to concentrate, lack of motivation, mood swings, dementia, phobias, delusions, suicidal ideation, memory loss, alterations in the accuracy of perceptions, visual and other hallucinatory distortions and more.
Many low thyroid sufferers may tend to be on the selfish side because they have a pervasive feeling of not having enough resources for themselves, much less enough to make the lives of any other people better. They sometimes tend to be cranky, abusive, stingy, critical, judgmental, and have a whole set of other exceedingly undesirable tendencies. They can suffer from lack of motivation or ambition and find it difficult to accomplish even simple tasks.
These folks know their feelings and behavior are quite inappropriate. They often feel frustrated, because in spite of their best efforts, there doesn’t seem to be much they can do to control these feelings, especially when the symptoms worsen during times of stress or just prior to the menstrual cycle.
It is often hard for them to find enjoyment in activities. They have a tendency to not feel like doing anything. They frequently can no longer find enjoyment in the things that they used to find quite interesting and enjoyable. For them, molehills frequently seem like mountains.
Why aren’t health professionals more informed about behavioral and psychiatric conditions resulting from a low thyroid condition?
Thyroid disease in general used to be treated by symptoms prior to the advent of the TSH test in the 1970s. People are now realizing this test does not detect many cases of low thyroid. It wasn’t until this lab test became the “gold standard” test for thyroid function that diseases like chronic fatigue syndrome, fibromyalgia, Irritable Bowel Syndrome and others came into existence. Many have surmised that these new “invisible diseases” are simply low thyroid conditions that are not being detected by the standard TSH test. Therefore it is quite possible that some psychiatric disorders are actually hypothyroid conditions which are not being detected by the TSH tests. So although a health professional may know about the link with behavioral/psychiatric conditions, the unreliable TSH test may cause them to rule out thyroid as an origin of the problems. Additionally, many health professionals think the TSH is the only test that is needed, and do not realize that thyroid antibodies alone can cause problems or that someone could be functionally hypo (low T3, normal TSH and Free T4).
Symptoms of Hypothyroidism
· Fatigue and low energy, with need for daytime nap.
· Depressed, down, or sad.
· Skin that becomes dry, scaly, rough, and cold.
· Hair becomes coarse, brittle, and grow slow.
· Excessive unexplained hair loss.
· Sensitivity to cold in a room when others are warm.
· Difficulty in sweating despite hot weather.
· Constipation that is resistant to magnesium supplementation.
· Difficulty in loosing weight.
· Unexplained weight gain.
· High cholesterol resistant to cholesterol lowering drugs.
____ I am gaining weight inappropriately
____ I'm unable to lose weight with diet/exercise
____ I am constipated, sometimes severely
____ I have hypothermia/low body temperature (I feel cold when others feel hot, I need extra sweaters, etc.)
____ I feel fatigued, exhausted
____ Feeling run down, sluggish, lethargic
____ My hair is coarse and dry, breaking, brittle, falling out
____ My skin is coarse, dry, scaly, and thick
____ I have a hoarse or gravely voice
____ I have puffiness and swelling around the eyes and face
____ I have pains, aches in joints, hands and feet
____ I have developed carpal-tunnel syndrome, or it's getting worse
____ I feel depressed
____ I feel restless
____ My moods change easily
____ I have feelings of worthlessness
____ I have difficulty concentrating
____ I have more feelings of sadness
____ I seem to be losing interest in normal daily activities
____ I'm more forgetful lately
____ I have worsening allergies
____ My hair is falling out
____ I can't seem to remember things
____ I have no sex drive
____ I am getting more frequent infections, that last longer
____ I'm snoring more lately
____ I have/may have sleep apnea
____ I feel shortness of breath and tightness in the chest
____ I feel the need to yawn to get oxygen
____ My eyes feel gritty and dry
____ My eyes feel sensitive to light
____ My eyes get jumpy/tics in eyes, which makes me dizzy/vertigo and have headaches
____ I have strange feelings in neck or throat
____ I have tinnitus (ringing in ears)
____ I get recurrent sinus infections
____ I have vertigo
____ I feel some lightheadedness
____ I have severe menstrual cramps
(collected from various places): The thyroid glad is located just below the adam’s apple. It regulates the energy output and metabolism of the body- low for sleep, medium for waking, high for physical activity. Also calcium levels are regulated by the thyroid (my kidney stone was made of calcium).
Hypothyroidism is the swelling of the thyroid. Symptoms are forgetfulness, fatigue, increased aggressive behavior, decreased affiliative behavior, low cognitive test scores, Alzheimer’s, brain aging, increased anxiety and stress, problems with memory and learning, thyroid enlargement, apathy, difficulty swallowing, and dry hair and skin.
Hypothyroidism & Body Temperature
Generally, the average temperature of an adult with a healthy thyroid is 98.6 degrees fahrenheit or 37.0 degrees celsius, and that occurs around mid-afternoon. To take your temperature, it’s important to have an accurate thermometer. Some digitals will give you a reading one degree less or more than a Mercury thermometer. So if you have any doubts about your digital thermometer, try an old-fashioned Mercury thermometer, which can be quite accurate if you leave it under your tongue long enough.When you’re hypo–and that includes EVEN being on the lousy T4-only medications, you can have a mid-afternoon temp in the 97’s, and a few I’ve read had their in the 96’s. BRRRR.So when you start on natural desiccated thyroid like Armour, and consistently raise your doses, you will see your temps climb over time, with matching feel-good symptoms to match.
But what if you are seeing your temperature all over the map, such as one temp one day, and a temp two degrees lower at the same time the next day?? That could be a sign that you have low-functioning adrenals, which means you aren’t producing enough cortisol. And for some folks, it takes supplementing with low-dose Hydrocortisone or other adrenal products to bring that stability in the temperature back.
· Thermal activity reflects metabolic activity. A low temperature means low metabolism and vice versa. For example, the temperature typically found in someone who is old, frail, pale and weak is low and typically ranges from 95 to 97 degrees if no infection is present. A healthy person will have an average temperature of 98.6 degrees, but may have a 100 degree or higher temperature in a hyperthyroid state or as high as a 104 to 105 degree temperature if there is a fever present these are high metabolic states.
· Wide variability in daily temperatures indicates a weak adrenal function since the adrenal glands help the body maintain stability. Good adrenal function produces a stable temperature. As adrenal function improves, the temperature variability decreases and vice versa. As adrenals get stressed (either from emotional stress, excess metabolic stimulation such as excessive thyroid stimulation, or for other reasons), the variability increases.
· In a hypothyroid state, the day-to-day averages are low and very stable. In a hypoadrenal state including adrenal exhaustion or adrenal stress, the temperatures are low and unstable -- one day they may average 96 degrees and one to two degrees higher the next day.
Causes of Hypothyroidism
Causes of Hypothyroidism
There are a variety of factors that can contribute to the development of thyroid problems: · Exposure to external radiation such as occurred after the Chernobyl nuclear plant accident.
· Over-consumption of isoflavone-intensive soy products such as soy protein or powder. Isoflavones act as potent anti-thyroid agents, and are capable of suppressing thyroid function, and causing or worsening hypothyroidism.
· Some anti-thyroid drugs, such as lithium and the heart drug cordarone.
· History of radiation treatment to the head and neck area.
· Over-consumption of uncooked "goitrogenic" foods, such as broccoli, turnips, radish, cauliflower, and Brussels sprouts.
· Radioactive iodine treatment for hyperthyroidism/Graves' Disease.
· Post-surgical removal of all or part of the thyroid due to nodules or cancer.
· Adrenal insufficiency (commonly caused by chronic stress).
· Mercury intoxication (amalgams are 50% mercury). Amalgam fillings have been associated with a variety of problems such as Alzheimer's disease, infertility, neurotransmitter imbalances, and thyroid problems.
As many as 10 percent of 98 million Americans with high cholesterol and high LDL ("bad") cholesterol may not know that their cholesterol is high due to undiagnosed thyroid problem. Older women with sub clinical or under-active hypothyroidism was shown to be twice as likely as women without this condition to have heart attacks.
Thyroid disease is also intricately tied to adrenal gland and ovarian function.
In hypothyroidism, the thyroid is not producing enough thyroid hormone. This may be due to autoimmune disease that makes it underactive, radiation or drugs that has partially or fully disabled the thyroid, or surgical removal of all or part of the thyroid. When you are hypothyroid, your thyroid doesn't produce any or enough thyroid hormones, and the missing hormone is replaced by thyroid hormone replacement drugs.
Soy can cause hypothyroidism because it has goitrogenic properties. See the section on Soy for more information. I eat probably three times as much soy protein isolate as you do. Not only do I eat it for dinner sometimes, but I have it via soy milk every time I eat cereal, and I have it for most of my lunches via chick patties and other veggie-burger-type things.
Connections to Gilbert's Syndrome
PERSONAL: Gilberts Web Forums
I have a theory I thought I'd post, and get your reactions. One of the main problems Gilberts sufferers seem to have is that doctors don't believe it causes any problems. I discovered I had Gilberts over 18 months ago, and I am still suffering badly - but not with Gilberts, rather chronic fatigue, or rather hypothyroidism and hypoadrenalism. In standard blood tests, Gilberts shows up, and is often casually dismissed by the doctor as a benign condition. Yet many of us suffer and cannot understand why Gilberts is ignored by the medical profession. I personally am devastated by this - I am a 39 year old female, struggling to bring up 3 small children with severe chronic fatigue, and have been dismissed as just having Gilberts. After much research, I understand Gilberts to be due to an enzyme shortage in the phase 2 pathway, which operates sluggishly. I believe this sluggishness also affects other processes that are performed in the phase 2 pathway, including the conversion of the thryoid hormones T4 to T3. Low thyroid levels will affect the phase 2 pathway efficacy, as well as the adrenals. Anecdotal evidence from these boards leads me to believe that many Gilberts people suffer hypothyroidism, ie, the rate of T4 to T3 conversion is slow, and so we are cold and fatigued, have anxiety, possible hypoadrenalism (don't produce enough cortisol) and hypoglycaemia. Sound familiar to anyone? Heavy metals also burden the phase 2 pathway (got any mercury fillings? they won't help your Gilberts or your thyroid).Some of us may end up on thyroid treatment (Synthroid, Euthyrox etc etc) but this does not solve the problem. As most of us have problems converting T4 to T3, giving us T4 alone will not help us much, and will possibly cause us to become hyper on a low dose. This happened to me at Christmas with a total adrenal crash. I believe a combination of T4 / T3 like Armour or Thyroid S will be much more helpful. I am about to start this treatment myself, and I will be reporting back on progress.
My theory is that so-called Gilberts symptoms - cold, fatigue, brain fog, anxiety, digestive problems, feeling lousy in the mornings, better in the evenings, headaches - are actually undiagnosed, and untreated thyroid problems. And we can try all we like to improve our liver function with juicing, milk thistle, liver diet, etc etc, and doubtless these will do no harm, but the real issue here may be hypothyroidism that may not show up on standard blood tests. Low thyroid levels affect the efficacy of the phase 2 pathway of the liver, and thus the bilirubin levels in GS sufferers.
PERSONAL: Gilberts Web Forums
If you are still troubled by fatigue, despite good diet, milk thistle etc etc, get your thyroid checked!! No amount of healthy eating will replace the hormones your body needs to function properly. Hypothyroid symptoms are identical to Gilberts syndrome - the yellow skin, digestive problems, fatigue, feeling cold, anxiety.Everything I have read says that the bulk of T4 / T3 conversion happens in the liver, though not specifically the phase 2 pathway. BUT -thyroid levels have an impact on the glucoronidation process which takes place in the phase 2 pathway. (This is from the book Amalgam Illness by Dr Andy Cutler - he suggests increasing thyroid levels in order to increase the glucoronidation process) This glucoronidation process is what breaks down the bilirubin in normal people, and is the process where the enzyme is lacking or less efficient in people with Gilberts. So, what I am saying is that low thyroid levels can hamper the glucoronidation process, and increase the build up of bilirubin.
I understand that T4 (thyroid hormone) is converted to T3 by the enzyme 5'-deiodinase, a process that also takes place in the liver. A sluggish liver will have difficulties with thyroid conversion as well.
So on a standard blood test, you may get 'normal' TSH / T4 results (which as you have probably read by now are next to useless) and elevated bilirubin, get the diagnosis of Gilberts, and 'there's nothing wrong with you, it's a benign condition', when in fact you are hypothyroid.
It is possible that the adrenals will also need to be treated, as the body needs cortisol to drive the T3 and T4 into the cells. If the adrenals aren't producing enough cortisol, the body won't be able to use the thyroid hormone. Hypoadrenalism is common with hypothyroidism - the working of the thyroid impacts the adrenals, and vice versa. If one is underperforming, the other will too. Treating just one, ie the thyroid, will cause stress on the adrenals, and can lead to adrenal collapse (I experienced this at Christmas - not pleasant). You may need to treat the adrenals first, then begin thyroid treatment.
PERSONAL: Gilberts Web Forums
During those episodes of debilitating fatigue and depression did you happen to take your temperature? Do you know what your average body temps are on a daily basis? If your temps fall below 97.8 consistently you are experiencing hypometabolism and the reason could be associated with that sluggish liver. The liver is responsible for converting T4 thyroid to the active form T3 which is required in every living cell. Conventional thyroid tests fail to identify this condition. Your body temps could still be low while your test results are within normal limits. I too experienced fatigue and depression (I have GS) until supplementing with T3 following Dr Denis Wilson's protocol: wilsonssyndrome.com/
My other symptoms relieved by T3:
Inability to get out of bed in the morning
Lack of self confidence
lack of motivation
PERSONAL: Gilberts Web Forums
I've just today had another diagnosis to add to my already hypochondriac-sounding list ........ it seems I'm also hypothyroid, which, after years of swollen thyroid gland makes sense, really. Apparently, this is what has been causing some of my digestive upsets, fatique and nausea, according to the hospital doctor. It went undiagnosed for years, as nothing showed up on blood tests, and the symptoms were milder. (Interestingly, I also have a tender liver today, noticed by the doctor on examination, and yellow eyes. But the bili is normal. Hmmm) On Sunday, I passed out at work, and this morning again, that's why I had this looked into today.
I'd been doing much better in general lately, though, after the anti-candida diet, and looking after myself better, etc.
I have just found out i have Gilberts syndrome after months of frustration of not knowing what was happening to me. I aslo have thyroid problems which i take 100mg of thyroxine.
I've noticed that a few of you guys also have the "lump in the throat" thing/thyroid problems (either suspected or diagnosed). I've had this condition for years (suspected, and now they say I HAVE a thyroid condition, but the details on that are fuzzy at the moment), plus GS, CFS, allergies, and digestive disturbances for all that time too.
I wonder how many of you have the throat problems, as I've just found out that thyroid problems can cause many digestive problems, fatigue, of course, allergies, shaking/trembling, nausea, dizziness, hair loss, etc. Sound familiar ?!?
PERSONAL: Gilberts Web Forums
I was diagnosed with hypothyroidism a couple of years after the official GS diagnosis. I did have thyroid checked not long before that and it was fine. Once I got on the thyroid meds I felt much better. I bet there's a link somewhere. I did have the amalgam fillings which have all been replaced with gold
I have learned a huge amount about hypothyroidism, mercury, the liver pathways, candida and treatments from Andy Cutler's book Amalgam Illness, available from Amazon. Expensive but really worth it for identifying and treating these issues. He states that the efficacy of the glucorinidation pathway (the culprit in Gilberts people) can be increased by raising thyroid hormones, ie that the Gilberts can be exacerbated by hypothyroidism, rather than Gilberts causing hypothyroidism.
I was diagnosed with Gilbert's syndrome hypothyroidism in the 1980s and am taking Synthroid. I have symptoms many of you write about--extreme fatigue, brain fogginess, difficulty concentrating, and long-standing memory problems... I suspect that there are a number of conditions that seem to co-occur and reading this forum was the first I realized that there is a good likelihood that Gilbert's and hypothyroidism co-occur at a higher rate than you would suspect and that they may be related.
T3 in Illness
High incidence of decreased serum triiodothyronine concentration in patients with nonthyroidal disease
Serum thyroxine (T4) and triiodothyronine (T3) concentration and binding were measured in 34 clinically euthyroid patients hospitalized for a wide variety of nonthyroidal diseases. Despite clinical euthyroidism, serum T3 was in the hypothyroid range (less than 90 ng/100 ml) in 24 of the 34 patients, and the mean serum T3 of this group, 78.4 +/- 38.3 (SD), was significantly decreased from that of control, 134.0 +/- 29.3 ng/200 ml. Mean serum T4 levels were essentially the same in both groups, 7.3 +/- 2.0 for sick patients and 7.2 +/- 1.0 mug/100 ml for the controls. Plasma binding of both T4 and T3 was decreased in the patient group to 69.9 and 78% of control values, respectively. In accord with previous studies, the mean free T4 index, proportional to free T4 concentration, was significantly increased to 10.0 +/- 4.1 in the patient group (control, 7.6 +/- 1.3). However, the mean free T3 index of the patient group, 92.9 +/- 38.4 remained decreased from that of control, 138.9 +/- 34.4. Of the 24 patients with decreased serum T3 (less than 90 ng/100 ml), low T3 levels could be attributed to decreased plasma binding in 8; in 5, serum T3 was within the normal range for their advanced age. Mean TSH was greater in the patient group 2.6 +/- 1.9, than in the controls, 1.9 +/- 1.1 muU/ml. Moreover, the TSH response to administered TRH was moderately exaggerated in 7 patients with low free T3 index compared to 7 patients with normal free T3 index. Although significant statistically, neither the basal nor TRH induced TSH levels were in the range generally found in primary hypothyroidism. The data suggest that the high incidence of low serum T3 (70%) and free T3 index (32%) in nonthyroidal disease may be related to the catabolic state that accompanies illness rather than to specific disease entities. At the present time, the use of serum T3 or free T3 measurements for the diagnosis of hypothyroidism does not appear justified in patients with nonthyroidal disease.
In Short: Patients with a wide variety of nonthyroid diseases showed much lower T3 levels (70% were in the hypothyroid range) while T4 levels remained normal. Plasma binding of T4 was 70% that of normal and T3 was 78% of normal. These findings may be due to the catabolic state that accompanies illness.
One of the other problems is the effect of the illness on thyroid functioning. It has long been noted that people are often functionally hypothyroid. That is, they produce enough thyroid hormones from the thyroid gland, as measured by levels in the blood, but they appear to be hypothyroid at a cellular level. This tends to occur in adult Fibromyalgia patients. Numerous effects could explain this:
1. The blood test for thyroid function is not a dynamic test, unlike, e.g. HbA1c. It simply represents what is in the blood, and not what is active at a cellular level. It is based on population sampling and would therefore include people with subclinical hypothyroidism. We will have to wait until the development of the nuclear membrane thyroid receptor volume test before we have a dynamic test of thyroid function. In medicine we tend to treat extremes and not subtle alterations in physiology. This means that people at the lower end of ‘normal’ are not treated. They may actually need to be at the upper end of normal, but the test will not tell you that. The body also has the ability, it seems, to keep the blood levels normal despite cellular thyroid problems. This can happen in any chronic illness.
2. In cytokine mediated illness the production of central and locally generated cytokines can affect the de-iodination pathways of thyroid hormones. It seems that high level of rT3, and low levels of T2 may ensue. Reverse T3 is a non-competitive inhibitor of T3 and is raised in stress situations. T2 is thought to be important for the functioning of mitochondria. High levels of rT3 have been found in post-operative patients subsequent to high cortisol output. It is thought to be an adaptive response in order to conserve energy. The situation of poor conversion of serum T4 to cellular T3, for whatever reason, has been called Wilson's Thyroid Syndrome.
3. Other hormones affect thyroid functioning. Cortisol is permissive for hormone uptake into cells and low cortisol levels can therefore have an effect on this. High cortisol can also inhibit functioning through its action on rT3 as mentioned above.
4. There is hypothalamic downregulation of the thyroid axis with altered sensitivity to TRH and TSH at their receptors
The treatment studies by Teitelbaum and Ali that I quote later both incorporated low dose thyroid hormone replacement in selected patients. This seems to be of great benefit especially to fibromyalgia patients, particularly borderline hypothyroid patients (T4 in lower 1/3 of reference interval TSH >3) or those with evidence of low T3.
THE THYROID IN NON-THYROIDAL ILLNESS
Elaine M. Kaptein, MD, FRCP(C), FACP
In the absence of hypothalamic, pituitary or thyroid diseases, systemic illnesses have multiple effects on thyroid hormone metabolism and on serum thyroid hormone concentrations (1-3). These changes are primarily related to the severity (2) (Figure ), and perhaps to the chronicity of illnesses (4), rather than to the specific disease states. Changes related to chronicity may be secondary to worsening malnutrition and/or catabolism which result in progressive declines in thyroid binding protein concentrations.
[A diagram shows that in mild illness, Total T4, Free T4, and reverse T3 are elevated, while Total T3 levels are decreased. In moderate illness, reverse T3 remains elevated, while Total T4 and Free T4 drop back into normal range. Total T3 levels are even more decreased. In severe illness, Total T3 is still more decreased, and Total T4 drops below the normal range. Here T4 and T3 binding also drops below normal range, and reverse T3 continues to rise]
Most frequently, serum levels of total T3 are reduced leading to the term “the low T3 syndrome” or “the low T3 state of nonthyroidal illness”. Less frequently, serum total and free T4 values and TSH concentrations are increased or decreased.
Serum total T3 concentrations are frequently reduced even with mild nonthyroidal disorders such as caloric deprivation, with the highest frequency and lowest values occurring in patients with the most severe illnesses (1, 2). Serum total T3 values return to normal only after complete recovery of the nonthyroidal illness and of the nutritional deficiency.
3) T4 uptake into rapidly equilibrating tissues like liver may be reduced in critically ill patients with NTIS (2).
4) Total T3 content of cerebral cortex, hypothalamus, anterior pituitary, liver, kidney, and lung are reduced in NTIS as is hepatic content of total T4; total hormone content may reflect primarily bound hormone (18).
5) T3 production rates are decreased in all NTIS patients (2)
Controversy exists as to whether the fall in total T4 concentrations during acute NTIS are primarily due to central suppression indicating hypothyroidism, to reduced serum T4 binding to TBG due to protease cleavage, indicating euthyroidism, or a combination of these factors (2, 6, 19). Wadwekar and Kabadi (20) addressed this question in a study of six euthyroid men with primary hypothyroidism maintained on L-T4 replacement therapy during an acute nonthyroidal illness. Prior to the illness, total T4, total T3 and TSH levels were in the reference range for euthyroid subjects. All of these values decreased during the acute illnesses, returning to pre-illness values with recovery (20).
Catabolisis is the process of a body breaking down the muscles and other tissues in your body in order to keep your vital processes working. Catabolisis will not begin until there are no usuable sources of energy coming into the body. Catabolisis will break down muscle tissue before it breaks down fat. Anabolism and catabolism are the two forces that make up metabolism.
The many biochemical processes that make up the body's metabolism can be grouped into two general categories - anabolism and catabolism. Anabolism is the building up of complex molecules, while catabolism is their breakdown. To build molecules and sustain life, the body needs energy. It gets this energy from the breakdown of nutrients such as glucose and fatty acids. So, for molecular construction to occur, molecular destruction must go on at the same time to release the energy required to drive the biochemical reactions. When anabolism exceeds catabolism, net growth occurs. When catabolism excesses anabolism net loss occurs.
Anabolism includes the chemical reactions that cause different molecules to combine to from larger, more complex ones. The net result of anabolism is the creation of new cellular material, such as enzymes, proteins, cells, cell membranes, and tissues. Anabolism is necessary for growth, maintenance, and tissue repair.
Catabolism includes the chemical reactions that break down complex molecules into simpler ones for energy production, for recycling of their molecular components, or for their excretion. If energy is produced, it is stored as glycogen or fat. Recently, the trend in sports nutrition has been to focus on anti-catabolic training methods and nutrients. For example, when the muscles are strenuously trained and the muscle fibers are damaged, cortisol is released at a higher level, speeding up the breakdown of tissues. Nutrients such as L-Glutamine have been shown to reduce the effects of cortisol, resulting in reduced tissue breakdown. Antioxidants and a number of phytochemicals also have anti-catabolic effects, as does high protein and all around good nutrition. By reducing the rate of catabolism, anabolism is increased, resulting in faster recovering, a higher level of performance, and an increased growth rate.
Note: Cortisol and exercise are known triggers for Gilbert's Syndrome. Could they be triggering a catabolic state which prevents T3 synthesis or breaks it down? For the first time in weeks, my temperature is down to 97.9 after a strong workout last night. Though it was 98.4 last night.
Tri-iodothyronine (T3) is produced by the peripheral deiodination of T4. T3 is much more potent than T4. About 99.5% of circulating T3 is bound (0.5% free). Reverse T3 is also produced by the deiodination of T4, but only when there is excess circulating thyroid hormone (hyperthyroid states). Reverse T3 is not physiologically active, so its production helps to prevent excess catabolism. Levels of reverse T3 are also elevated during periods of severe illness.
Bilirubin & Albumin Saturation
An interesting thing I've been looking into as well - albumin is the blood serum carries many things, but large among them are bilirubin and thyroid hormones. And different things compete for space in albumin. Meaning that higher bilirubin counts probably prevent the albumin from carrying as much T4 and T3 hormones.
REFERENCE: Wikipedia - Serum Albumin
Serum albumin, often referred to simply as albumin is the most abundant plasma protein in humans and other mammals. Albumin is essential for maintaining the oncotic pressure needed for proper distribution of body fluids between intravascular compartments and body tissues.
Functions of Albumin
Maintains osmotic pressure
Transports thyroid hormones
Transports other hormones, particularly fat soluble ones
Transports fatty acids ("free" fatty acids)
Transports unconjugated bilirubin
Transports many drugs
Competitively binds calcium ions (Ca2+)
Elevated concentrations of albumin in plasma are caused by a relative loss of water. This occurs in dehydration, or with prolonged use of a tourniquet. There are no pathological conditions other than dehydration associated with a high albumin concentration. Note however that elevated albumin may indicate artefactual elevation of other analytes such as haemoglobin, lipids and calcium.
Concentrations of PFOS required to saturate albumin would be in excess of 50 to 100 mg/L. Based on current environmental concentrations, it is unlikely that PFOS would cause displacement of hormones from serum proteins in wildlife.
Note: implies that albumin can be saturated, and that its saturation with one thing prevents it from transporting other things. For example, when saturated with bilirubin, transportation of energy or thyroid hormones may be diminished.
The cytoxicity of bilirubin cannot be accurately assessed from its total concentration in plasma, because bilirubin is bound to albumin. The current studies demonstrate the ability of albumin to bind bilirubin is significantly reduced when other organic anions (e.g. sulfisoxazole, benzoate, and hematin, which also bind to albumin) coexist in the plasma of neonatal infants with hyper-bilirubinemia. The results indicate that the pathogenesis of bilirubin toxicity is more closely related to that fraction of the circulating bilirubin which is dissociated from albumin or indirectly to the relative saturation of the albumin with bilirubin.
SCIENCE: National Library of Medicine
The influence of fatty acids on the binding of bilirubin to albumin.
The influence of free fatty acids (FFA's) on the albumin binding of bilirubin was studied in vitro in the plasma of infants with neonatal hyperbilirubineamia and in solutions employing crystalline albumin to which bilirubin and FFA (oleic acid) were added. The bilirubin saturation index (SI) was utilized to distinguish between that fraction of bilirubin bound at the primary (high-affinity) site of albumin and bilirubin bound at secondary sites from which it is easily dissociated by salicylate. The relative saturation of albumin with bilirubin was also measured by addition of salicylate to whole blood samples where bilirubin was also measured by addition of salicylate to whole blood samples where bilirubin dissociated from the albumin could be sequestered by the red cells. The present studies indicate that FFA's influence the binding of bilirubin in two ways. At molar ratios of FFA to albumin (2:1 to 4:1), the FFA's compete with bilirubin for binding at the high-affinity site so that a significant portion of the bilirubin is transported at secondary sites, making it susceptible to displacement by water-soluble organic anions. At high molar ratios (greater than 5:1) FFA's compete with bilirubin for albumin binding at the secondary sites as well. In contrast to crystalline albumin where the first two molar equivalents of FFA do not influence the binding of bilirubin to albumin, all FFA concentrations in hyperbilirubinemic plasma reduce the affinity of albumin for bilirubin at its high-affinity site even though there is a molar excess of albumin over bilirubin.
One gram of adult albumin will bind very tightly at its high affinity binding sites approximately 8 mg of bilirubin. Additional bilirubin can bind to secondary sites on albumin; but these latter complexes have a binding constant approximately two orders of magnitude lower than the high affinity binding sites on the albumin (5).
Reasons why bilirubin may enter brain:
1. Excess bilirubin production which overwhelms albumin and other blood buffering capacity.
Unconjugated bilirubin> nonpolar, lipophilic, binds to albumin in plasma (and RBC/platelet membranes and b-globulin); free
U-bili normally soluble at ~1 mM-->when binding capacity exceeded, free U-bili in plasma rises
One molecule of albumin binds 2 molecules bilirubin (1st is more tightly bound); at 1:1 molar ratio, 1 g albumin binds 8.4 mg
serum alb max binding capacity (1, 2 sites)
4.0 g/dl 33.6 mg/dl 77.2 mg/dl
3.5 29.4 58.5
3.0 25.2 50.4
2.5 21.0 42.0
Other factors which decrease U-bili binding to albumin:
1. Free fatty acids (sepsis, IV lipid emulsions)
2. Sulfa drugs (e.g., Bactrim)
Peripherally arising bilirubin is transported to the liver in association with albumin, where the remaining catabolic reactions take place.
Under physiological conditions, bilirubin remains bound to serum albumin which carries it to the liver for further metabolism. However, when bilirubin-to-albumin molar ratio (B/A) exceeds 1 : 1, free bilirubin binds to many types of cells including brain cells which is the cause of brain toxicity in premature neonates, a condition called kernicterus or bilirubin encephalopathy. In addition, jaundiced neonates with low plasma pH have been reported to be at greater risk of developing bilirubin encephalopathy (Kim et al 1980). Interaction of bilirubin with cells or cell membranes is well documented (Bratlid 1972; Sato et al 1987; Vazquez et al 1988; Hayer et al 1989; Leonard et al 1989; Tayyab and Ali 1995, 1997) and it is commonly accepted that the toxicity of bilirubin depends on its passage across the plasma membrane and its association with membrane lipids (Ali and Zakim 1993; Zucker et al 1994).
At a given pH, increase in the B/A from 0.5 to 3.0 led to an increase in the membrane-bound bilirubin (figure 1). This increase was smaller up to a B/A of 1.5 : 1 but became more significant (P < 0.05) at high B/As at all the pH values used in this study. Nearly two-fold (P < 0.05) increase in membrane-bound bilirubin was noticed on increasing the B/A from 1.0 to 2.0... The amount of membrane-bound bilirubin at any B/A in the range of 0.5 to 3.0 was different at different pH values, being negatively correlated with pH of the medium. In other words, lowering the pH from 7.8 to 7.0 resulted in increased binding of bilirubin to erythrocyte membranes at all the B/As tested even if B/A was below 1 : 1.
Within the temperature range of 27°C to 37°C, the amount of membrane-bound bilirubin at any given B/A above 1 : 1 was found to be minimum. Increase in temperature on either side led to an increase in bilirubin binding to erythrocyte membranes at all B/As. Sato and Kashiwamata (1983) also reported minimum binding of bilirubin to erythrocyte membranes at 37°C using a B/A of 2.0. A comparison of bilirubin binding patterns of human erythrocyte membranes at different temperatures and B/As shows that at each temperature, the binding was higher at higher B/As. This unusual behaviour of bilirubin binding to erythrocyte membranes at different temperatures may be either due to the effect of temperature on the binding of bilirubin to albumin or due to the change in the physical state of bilirubin binding sites of the erythrocyte membranes.
In Short: Albumin carries bilirubin to the liver for metabolism. However, when bilirubin exceeds albumin, it will bring to many types of cells, including brain cells. Lower blood pH causes higher binding of bilirubin to membranes. Temperatures outside the range of 27°C (80.6°F) to 37°C (98.6°F) also increased bilirubin binding to membranes.
Drugs That Displace Bilirubin From Albumin
Drugs Which Displace Bilirubin From Serum Albumin
Drugs that decrease bilirubin measurements include barbiturates, caffeine, penicillin and high dose salicylates.
Note: Not sure of the action involved in each of these - some may actually help conjugate and excrete bilirubin, while others might simply displace it from albumin and affect the measurement.
Note: These two taken together seem to imply that bilirubin is only picked up in tests when bound to albumin.
REFERENCE: Wikipedia - Salicylates
Salicylic acid is a colorless, crystalline organic carboxylic acid. It is usually prepared by Kolbe synthesis (aka Kolbe-Schmitt reaction). Salicylic acid functions as a plant hormone.
Also known as Beta Hydroxy Acid (compare to AHA), salicylic acid is the key additive in many skin-care products for the treatment of acne, psoriasis, callouses, corns, keratosis pilaris and warts. It treats acne by causing skin cells to slough off more readily, preventing pores from clogging up. This effect on skin cells also makes salicylic acid an active ingredient in several shampoos meant to treat dandruff.
Aspirin (acetylsalicylic acid or ASA) can be prepared by the esterification of the phenolic hydroxyl group of salicylic acid.
Subsalicylate in combination with bismuth form the popular stomach relief aid known commonly as Pepto-Bismol. When combined the two key ingredients help control diarrhea, nausea, heartburn, and even gas. It is also very mildly anti-biotic.
SCIENCE: National Library of Medicine
Salicylates are used to relieve pain and reduce fever. Most salicylates are also used to relieve some symptoms caused by arthritis (rheumatism), such as swelling, stiffness, and joint pain. However, they do not cure arthritis and will help you only as long as you continue to take them.
Note: This is a good resource
http://www.clinchem.org/cgi/content/abstract/33/4/597 (this is copied from the Thing That Help section on caffeine)
By means of gel-filtration of bilirubin/albumin mixtures, it is shown that unconjugated bilirubin remains completely linked to albumin (both human and bovine) in tetraborate buffer (pH 9.3), protein-free bilirubin appearing only when the bilirubin/albumin molar ratio exceeds two. On the other hand, bilirubin is completely set free from its protein link in the caffeine reagent. Additional chromatographic and spectrophotometric evidence is reported indicating the formation of a low-affinity complex between bilirubin and caffeine. These data explain why the spectrophotometric properties of bilirubin/albumin mixtures are matrix-dependent if measured in the tetraborate buffer but are no longer so when measured in the caffeine reagent.
In Short: Caffeine separates unconjugated bilirubin from albumin. The bilirubin then weakly binds to the caffeine. This leads to lower (from what I've read elsewere) measurements of bilirubin. But I wonder if this doesnt also free the albumin to be a carrier for thyroid hormones, which increases energy in a completely different way - a way in which those with GS are lacking.
[Fluoride] is an enzyme poison. Enzymes are complex protein compounds that vastly speed up biological chemical reactions while themselves remaining unchanged. As you read this, there is occurring in all of us a vast multitude of these reactions to maintain life and produce the energy to sustain it. The chains of amino acids that make up these complex proteins are linked by simple compounds called amides; and it is with these that fluorine molecules react, splitting and distorting them, thus damaging the enzymes and their activity. Let it be said at once, this effect can occur at extraordinary low concentrations; even lower than the one part per million, which is the dilution proposed for fluoridation in our water supply.
Moreover, fluorides are cumulative and build-up steadily with ingestion of fluoride from all sources, which include not just water but the air we breathe and the food we eat. The use of fluoride toothpaste in dental hygiene and the coating of teeth are further sources of substantial levels of fluoride intake. The body can only eliminate half of the total intake, which means that the older you are the more fluoride will have accumulated in your body.
What is the result of these toxic effects?
First the immune system. The distortion of protein structure causes the immune proteins to fail to recognise body proteins, and so instigate an attack on them, which is Autoimmune Disease.
Musculoskeletal damage results further from the enzyme toxic effect; the collagen tissue of which muscles, tendons, ligaments and bones are made, is damaged.
What concerns me so deeply is that in concentrations as low as 1ppm, fluorides damage the thyroid system on 4 levels.
1. The enzyme manufacture of thyroid hormones within the thyroid gland itself. The process by which iodine is attached to the amino acid tyrosine and converted to the two significant thyroid hormones, thyroxine (T4) and liothyronine (T3), is slowed.
2. The stimulation of certain of the G proteins whose function is to govern uptake of substances into each of the cells of the body, from the toxic effect of fluoride, has the effect of switching off the uptake into the cell of the active thyroid hormone.
3. The thyroid control mechanism is compromised. The thyroid stimulating hormone output from the pituitary gland is inhibited by fluoride, thus reducing thyroid output of thyroid hormones.
4. Fluoride competes for the receptor sites on the thyroid gland which respond to the thyroid stimulating hormone; so that less of this hormone reaches the thyroid gland and so less thyroid hormone is manufactured.
These damaging effects, all of which occur with small concentrations of fluoride, have obvious and easily identifiable effects on thyroid status. The running down of thyroid hormone means a slow slide into hypothyroidism. Already the incidence of hypothyroidism is increasing as a result of other environmental toxins and pollution together with wide spread nutritional deficiencies.
GS & The Lump in the Throat
There are also several accounts, including my own, of a lump in the throat in the vicinity of the thyroid gland. Take a look in the Symptoms section.
PERSONAL: Gilberts Web Forums
I have just read a book about a woman who was hypothyroid for 23 years, and it wasn't picked up by the doctors because they go by the TSH blood test only, not the free T3 and T4 levels as well as clinical observation. She was totally debilitated, ended up in a wheelchair for years, and finally got a proper thyroid assessment. After taking Armour for 12 days, her brain fog lifted, and she recovered slowly. She is now completely fine.
The last one in particular will interest you. If you cannot get a doctor to measure Free T3 and T4 levels, you can do it yourself via a 24 hour urine test. The Free T3 and T4 blood tests are in themselves reliable, but they need sensitive interpretation by an informed doctor. I strongly recommend you read the Tears Behind Closed Doors book - this gives a lot of detail about the problems with blood tests.
TSH is felt by the medical profession to be the gold standard of measuring thyroid function. Patients and informed doctors deride it as meaningless, as it only measures the level of thyroid stimulating hormone in the blood, not the actual levels of T3 and T4 at cellular level. It is possible to be hypothyroid and still well within range of the TSH blood test.
This is why Free T3 and T4 levels need to be tested. But it is possible for these results to be in range, and for the patient to be hypothyroid. This is where an intelligent and sensitive clinical evaluation of symptoms by the doctor comes in. No dismissing the patient's symptoms as depression, or neurotic. But actually LISTENING to what she is saying. My Free T3 and T4 levels are in range, but only just. I have debilitating hypothyroid symptoms.
This panel is used to evaluate thyroid function. The combination of the serum T4 and T3 uptake (THBR) as an indirect assessment of thyroxine-binding globulin (TBG). TBG helps to determine whether an abnormal T4 value is due to alterations in serum thyroxine-binding globulin or to changes of thyroid hormone levels. Deviations of both tests in the same direction usually indicate that an abnormal T4 is due to abnormalities in thyroid hormone. Deviations of the two tests in opposite directions provide evidence that an abnormal T4 may relate to alterations in TBG. This panel consists of the following tests:Thyroid-Stimulating Hormone (TSH), Free Tri-iodothyronine (T3) free, Thyroxine (T4)
• Thyroid-Stimulating Hormone (TSH)
This test is used to identify primary hypothyroidism and to differentiate it from secondary (pituitary) and tertiary (hypothalamus) hypothyroidism.
• Triiodothyronine (T3), Free, Serum
This test is used to evaluate thyroid function. It is primarily used to diagnose hyperthyroidism. It is also used to assess abnormal binding protein disorders and to monitor thyroid replacement and suppressive therapy
• Thyroxine (T4)
This test is used to evaluate thyroid function. T4 is decreased in hypothyroidism and in the third stage of subacute thyroiditis. T4 is increased with hyperthyroidism, subacute thyroiditis in its first stage and with thyrotoxicosis due to Hashimoto disease. T4 is also used to diagnose toxicosis.
The thyroid gland uses iodine from food to make two thyroid hormones, thyroxine (T4) and triiodothyronine (T3). The thyroid gland stores these thyroid hormones and releases them as they are needed.
• Thyroxine (T4) is produced by your thyroid gland when the pituitary gland releases thyroid-stimulating hormone.
• Only a small amount of triiodothyronine (T3) is produced directly by your thyroid gland. Most T3 is made by other tissues that convert T4 into T3.
Thyroid hormone blood tests include:
• Free thyroxine index (FTI or FT4). Free thyroxine (T4) can be measured directly (FT4) or calculated (FTI). The FTI is a measure of the amount of T4 in relation to the amount of thyroxine-binding globulin present. The FTI is calculated from the T4 and T3 uptake, or T3U, values. The FTI value can indicate when an abnormal level of T4 is caused by an abnormal level of thyroxin-binding globulin in the blood.
• Triiodothyronine (T3). T3 has a greater effect on metabolism than T4, even though T3 is normally present in lower amounts than T4. The total amount of T3 in the blood or the amount of free T3 (FT3) can be measured. Normally, less than 1% of the T3 is free.
• Triiodothyronine uptake (T3U). The T3U test is an indirect measurement of the amount of the protein (thyroxine-binding globulin) that can bind to T3 and T4. The results of this test are useful only when evaluated along with other thyroid function tests.
• Total Thyroxine (T4). Most of the T4 in blood is attached to a protein (called thyroxine-binding globulin). Less than 1% of the T4 is unattached. A total T4 blood test measures both bound and free thyroxine. Free thyroxine affects tissue function in the body, but bound thyroxine does not.
Note: I was not tested for T3. Just T3 uptake.
My test results:
TSH: 1.907 (0.35-5.5)
Thyroxine (T4): 8.9 (4.5-12.0)
T3 Uptake: 30 (24-39)
Free Thyroxine Index: 2.7 (1.2-4.9)
Thyroid Peroxidase (TPO) Ab: <10 (0-34)
Thyroid Antithyroglobulin Ab: <20 (0-40)
TSH: Reflects the blood level of thyroid stimulating hormone.Total T4: Reflects the total amount of T4 present in the blood, i.e., the protein bound (unavailable) T4 and the Free T4. Note that high levels of estrogens (birth control pills or pregnancy) can increase the amount of the protein that binds T4; giving misleading elevated Total T4 values which can look like ‘hyperthyroidism’ when it is not.Total T3: Reflects the total amount of T3 present in the blood, i.e., the protein bound (unavailable) T3 as well as the Free T3. Again, high estrogen levels create the same effect as mentioned in relationship to T4 above.Free T4: Reflects the biologically active (free) form of T4. This T4 can be converted to T3 or RT3. In the presence of elevated estrogen levels, the Free T4 gives a more accurate assessment of thyroid function.Free T3: Reflects the biologically active (free) form of T3 that can generate production of energy (in the form of ATP). In the presence of elevated estrogen levels, the free T3 gives a more accurate assessment of thyroid function.
T3 Uptake: This test is mentioned only as a warning not to use it. In fact, it does not measure T3 levels at all -- the name is misleading. It is an old test that was developed before we were able to accurately measure T4 levels. The assumption was that if the patient had a high T4 level, the blood proteins would be saturated with it. Therefore when mixed with T3 (which is easier to measure), the proteins would take up very little T3. Thus a low T3 uptake implies elevated T4 levels and vice versa. Thus the T3 Uptake test is actually an antiquated, inaccurate way to measure T4 levels.
Old Laboratory Tests Unreliable
Most all older thyroid function panels include the following:
• Total T4
• T3 Uptake and
• Free Thyroxine Index (FTI).
These tests should be abandoned because they are unreliable as gauges of thyroid function. The most common traditional way to diagnose hypothyroidism is with a TSH that is elevated beyond the normal reference range. For most labs, this is about 4.0 to 4.5. This is thought to reflect the pituitary's sensing of inadequate thyroid hormone levels in the blood which would be consistent with hypothyroidism. There is no question that this will diagnose hypothyroidism, but it is far too insensitive a measure, and the vast majority of patients who have hypothyroidism will be missed.
Basal Body Temperature
Basal body temperature popularized by the late Broda Barnes, M.D. He found the clinical symptoms and the body temperature to be more reliable than the standard laboratory tests was provided. This is clearly better than using the standard tests. However there are problems with using body temperature.
• Sleeping under electric blankets or water beds falsely raise temperature
• Sensitive and accurate thermometer required
• Inconvenient and many people will not do (poor compliance)
New and More Accurate Way To Check for Hypothyroidism
This revised method of diagnosing and treating hypothyroidism seems superior to the temperature regulation method promoted by Broda Barnes and many natural medicine physicians. Most patients continue to have classic hypothyroid symptoms because excessive reliance is placed on the TSH. This test is a highly-accurate measure of TSH but not of the height of thyroid hormone levels.
New Range for TSH to Diagnose Hypothyroidism
The basic problem that traditional medicine has with diagnosing hypothyroidism is the so-called "normal range" of TSH is far too high: Many patients with TSH's of greater than 2.0 (not 4.5) have classic symptoms and signs of hypothyroidism (see below).
• So, if your TSH is above 2.0 there is a strong chance your thyroid gland is not working properly.
Free Thyroid Hormone Levels
One can also use the Free T3 and Free T4 and TSH levels to help one identify how well the thyroid gland is working. Free T3 and Free T4 levels are the only accurate measure of the actual active thyroid hormone levels in the blood.
When one uses free hormone levels one will find that it is relatively common to find the Free T4 and Free T3 hormone levels below normal when TSH is in its normal range, even in the low end of its normal range. When patients with these lab values are treated, one typically finds tremendous improvement in the patient, and a reduction of the classic hypothyroid symptoms.
Secondary or Tertiary Hypothyroidism
There are a significant number of individuals who have a TSH even below the new 1.5 reference range mentioned above, but their Free T3 (and possibly the Free T4 as well) will be below normal. These are cases of secondary or tertiary hypothyroidism, so, TSH alone is not an accurate test of all forms of hypothyroidism, only primary hypothyroidism.
UNDERARM TEMPERATURE TEST FOR HYPOTHYROIDISMINSTRUCTIONS:
1. Use any mercury thermometer. Shake it down the night before to 96 degrees or less and put it by your bedside.
2. In the morning, as soon as you wake up, put the thermometer deep in your armpit for ten minutes and record the temperature. Do this before you get out of bed, have anything to eat or drink, or engage in any activity. This will measure your lowest temperature of the day, which correlates with thyroid gland function. The normal axillary temperature is 97.8-98.2 degrees F. we frequently recommend treatment if the temperature averages 97.4 or less. The temperature should be taken for five days. However, if the temperature is 97.0 or less for three consecutive days, you do not need to take the last two temperatures. The axillary (underarm) temperature is used because oral (mouth) temperature does not correlate closely with thyroid function.
3. For women, the temperature should be taken starting the second day of menstruation. That is because a temperature rise occurs around the time of ovulation which may lead to incorrect interpretation of the test. If you miss a day, that is OK, but be sure to finish the testing before ovulation. For men, and for women who are menopausal, it makes no difference when the temperatures are taken. However, do not do the test when you have an infection or any
other condition that would raise your temperature.
There is considerable evidence that blood tests often fail to detect hypothyroidism (underactive thyroid). It appears that many individuals have "tissue resistance" to thyroid hormone. Therefore, your body may need more thyroid hormone, even though the amount in your blood is normal. A low axillary temperature suggests (but does not prove) hypothyroidism. We frequently recommend a therapeutic trial with a natural thyroid medication for individuals who have typical hypothyroid signs and symptoms and a low body temperature. This approach to thyroid therapy is controversial and is currently outside of the medical mainstream. However, we have found this method to be safe when properly administered, and in some cases it is the most effective or the only effective treatment for certain chronic problems.
SIGNS AND SYMPTOMS ASSOCIATED WITH HYPOTHYROIDISM:
Fatigue, depression, difficulty concentrating, difficulty getting up in the morning, cold hands and feet or intolerance to cold, constipation, loss of hair, fluid retention, dry skin, poor resistance to infection, high cholesterol, psoriasis, eczema, acne, premenstrual syndrome, loss of menstrual periods, painful or irregular menstrual periods, excessive menstrual bleeding, infertility (male or female), fibrocystic breast disease, and ovarian cysts.
POSSIBLE SIDE EFFECTS:
We consider thyroid hormone to be safe when administered properly. Occasionally, people taking thyroid hormone experience nervousness, rapid pulse, insomnia, and (on rare occasions chest pain. If any of these side effects occur, reduce the dose and call the office.
Since the 1970’s several new health issues and diseases have been “discovered”. In 1980, Chronic Fatigue Syndrome and Fibromyalgia were first noted. High cholesterol wasn’t considered a widespread health problem until the 1970’s, and Depression has become an epidemic. In 1982, Osteoporosis also became a health issue. In fact, all these health issues have become closely related to undiagnosed or undertreated hypothyroidism.The TSH (thyroid stimulating hormone) test was created in 1973. It is used to diagnose thyroid problems, but it measures a hormone from the pituitary gland, not the thyroid. A feedback loop exists in your body where the pituitary gland produces more or less thyroid stimulating hormone in response to the level of thyroid hormones in the bloodstream, and the thyroid produces more or less hormone based on the level of TSH. The normal range for the TSH test has been lowered several times, (the AACE, American Association of Clinical Endocrinologists, now recommends a range from 0.3 to 3.0), yet patients are not diagnosed until the TSH is much higher than the 3.3. In the case of autoimmune thyroid problems, the TSH can be within the normal range, yet antibodies are attacking the thyroid. Even the AACE estimates that as many as 1 in 5 Americans suffers from hypothyroidism.
A human thyroid produces T4, T3, T2, T1 and calcitonin. For nearly 100 years, hypothyroid patients were given desiccated porcine thyroid (dried thyroid gland from pigs), and doses were increased until all symptoms were gone. Synthroid became the treatment of choice for hypothyroidism by the 1970s. This new drug contains only the storage thyroid hormone known as T4, leaving patients undertreated.
PERSONAL: Gilberts Web Forums
Get a blood test from the doctor to measure TSH, T4, T3, cortisol and DHEA levels. Something may show up there - but blood tests are very unreliable in showing up problems - you may have all the correct levels of hormones circulating in your blood, but they may not be doing their job where they should. You may have high levels of Reverse T3 which is preventing the T3 from doing its job. Burned out adrenals from continued stress will produce only low levels of cortisol, and can give you all sorts of problems, including fatigue, and hypoglycaemia.
Treatments for Hypothyroidism
A study published in the New England Journal of Medicine in 1999 (see article now) suggested that brain T4 to T3 conversion may be impaired in some patients and that a select group of patients should be treated with both T4 and T3. Other studies published in the Journal of Clinical Endocrinology and Metabolism in 2003 (see article now) suggested that addition of T3 to T4 treatment is not needed for most patients with primary hypothyroidism. I recommend that most patients be started on a T4 preparation, which improves symptoms in the large majority of the patients. I have found that most patients prefer Levoxyl or Unithroid to Synthroid, but this varies with each patient.
After initial treatment with T4, I adjust their T4 dose until their TSH is between 0.5 and 2 mU/mL. If they remain symptomatic despite an optimized TSH, then low doses of T3 given two or three times a day can be added cautiously to T4. If patients start with a low blood free T3 level, then I am more inclined to treat them with T4 plus T3. On T4 plus T3 therapy, I use blood tests to make sure the free T4 and free T3 are in the upper-normal range. The TSH value is usually suppressed on combination treatment.
PERSONAL: Gilberts Web Forums
How to treat hypothyroidism is a whole other medical controversy. Your standard GP will look at your TSH, and if it is over 4, prescribe give you synthetic T4 medications. Firstly,the TSH is meaningless - you need to get your free T3 and T4 levels checked - and even if these are within range but at the low end, it is likely that you will benefit from T3/T4 combo treatment ie Armour or Thyroid S.
I am now also taking a T3 T4 combination thyroid medication, and the difference is amazing. From being totally debilitated just a few weeks ago, I am now much brighter and able to do much more without becoming exhausted. I feel almost normal. I still have a long haul ahead - I am half way through removing my amalgams - and I then have chelation to consider - but taking proper thyroid meds has given me my life back. I am so grateful.
PERSONAL: Gilberts Web Forums
Well, there seems to be a connection with hypothyroidism and GS. When I when for a bloodtest to have my thyroid checked out, the TSH levels were around 7. And followed another test a month later to have the reading just over 3. Apparently when doctors treat you for this their main goal is to get you in between 1 - 2. Since my last reading sat below 4 (reference is 0.32 - 4). I asked the doc if I could have a third test just to make sure, and he said no. So I have had to take measures into my own hands and take iodized (iodine) sea salt (still continueing with a good diet). I have felt much better than I have felt since I had this problem. I hardly get fatigued, and I haven't had an irregular heart-beat for some time now. I am actually starting to work now. I feel motivated enough to do so. So I would recommend getting iodine into your diet, as it gets converted into the required hormones in the bloodstream.
you need to be careful with iodine. It is not always the best thing for hypothyroidism, especially if you have Hashimotos.
Here you will be told how to monitor your own symptoms, take your temperature and slowly and responsibly treat yourself. You can post your blood test results and get a view from very knowlegeable hypothyroid sufferers whether you would benefit from thyroid hormone. You can buy generic Armour online if you cannot get a doctor's prescription. Email me on firstname.lastname@example.org if you want the address. But you must research this issue thoroughly, know the pitfalls, go slowly and what to expect. Body temperature is a dead giveaway - optimum body metabolism is 98.6 - if you are consistently below that you are likely to be hypothyroid.
Thyrolar and Armour include T3 and T4 hormones.
Levoxyl and Synthroid have T4 only.
Connections - Wilson's Syndrome
Note: This seems scammy, but interested in T3
We have found that a low body temperature is a strong indication that there is something wrong that can be fixed, particularly with the WT3 protocol and/or WTSmed Supplements. Just like a fever (high body temperature) is a good indicator that "something's wrong" and can cause people to feel terrible, so can a low body temperature. In fact, a low body temperature is more than enough to explain almost all of the health problems listed to the left. (below)
Headaches & Migraines
Easy Weight Gain
Anxiety & Panic Attacks
Low Sex Drive
Dry Skin & Hair
Cold Intolerance /
Carpal Tunnel Syndrome
When I began taking the liothyronine [T3 compound], I literally felt better immediately and within a few days felt better than I had ever felt in my life. The fatigue was gone, the headaches were gone, and the depression was gone.
Perhaps even more phenomenal, was that days prior to my first menstrual cycle after beginning the medication, I, for the first time in as long as I could remember, experienced no discomfort whatsoever- no mood swings, no cravings, no depression, no irrational behavior, and no cramping. Needless to say I was ecstatic and was almost non-believing that I could feel so generally good. -- Suzanne G.
Wilsons Doctors Listings:
Some of these symptoms can, in fact, be due to true hypothyroidism... The "Wilson's syndrome" website states that Dr. Wilson named this concept after himself "because it had not been previously described." In fact, for more than a century, the same set of symptoms has been given different names and attributed to a variety of causes by others, including the syndromes of neurasthenia, chronic fatigue, fibromyalgia, multiple chemical sensitivity, chronic Ebstein Barr disease, and chronic candidiasis.
Note: This apparently acknowledges the similarity between the symptoms of CFS, neurasthenia, fibromyalgia, multiple chemicle sensitivity, and candidiasis. The site argues against the existence of Wilson's Syndrome, but the argument is weak.